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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [FB5P-seq_C57Bl6]

ABSTRACT: Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [FB5P-seq_C57Bl6]

PROVIDER: PRJNA635287 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11853732_1.fastq.gz	Fastqsanger.gz
	SRR11853732_2.fastq.gz	Fastqsanger.gz
	SRR11853733_1.fastq.gz	Fastqsanger.gz
	SRR11853733_2.fastq.gz	Fastqsanger.gz
	SRR11853734_1.fastq.gz	Fastqsanger.gz

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [Ss2_pDC1]

Project description:The aim of the project is to characterize the heterogeneity of murine plasmacytoid dendritic cells (pDCs) and to decipher their activation trajectory during a viral infection in vivo. To this end, individual splenic pDCs were transcriptionally profiled at ground state and at the time of their peak production of type I interferon (IFN-I) during mouse cytomegalovirus (MCMV) infection, with enrichment of IFN-I-producing pDCs based on the use of a reporter mouse strain.

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [FB5P-seq_kinetic]

Project description:The aim of the project is to characterize the heterogeneity of murine plasmacytoid dendritic cells (pDCs) and to decipher their activation trajectory during a viral infection in vivo. To this end, individual splenic pDCs were transcriptionally profiled at ground state and at different times during mouse cytomegalovirus infection, with enrichment of IFN-I-producing pDCs based on the use of a reporter mouse strain and on their downregulation of LIFR.

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [Ss2_pDC2]

Project description:The aim of the project is to characterize the heterogeneity of murine plasmacytoid dendritic cells (pDCs) and to decipher their activation trajectory during a viral infection in vivo. To this end, individual splenic pDCs were transcriptionally profiled at ground state and at the time of their peak production of type I interferon (IFN-I) during mouse cytomegalovirus infection, with enrichment of IFN-I-producing pDCs based on the use of a reporter mouse strain and on their down-regulation of LIFR.

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection

Project description:Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [Ss2_pDC2]

Project description:Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [Ss2_pDC2]

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [Ss2_pDC1]

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [FB5P-seq_kinetic]

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Single-cell analysis of mouse plasmacytoid dendritic cells (pDCs) unravels their activation trajectory and their molecular regulation in vivo during a viral infection [FB5P-seq_C57Bl6]

Project description:The aim of the project is to understand the heterogeneity of murine plasmacytoid dendritic cells (pDC) for interferon I production. For this end we want to perform RNAseq on splenic pDC at ground state and also after infection of mice with MCMV at different time points.

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RNA-seq analysis of activated plasmacytoid dendritic cell subsets after viral infection

Project description:Hematopoiesis generates cell diversity through evolutionarily-determined differentiation programs defined at steady-state conditions. Here, we show that peripheral innate immune activation can generate cell diversity and functional specialization during the activation process. We found that activation of steady state human plasmacytoid pre-dendritic cells (pDCs) with a single microbial stimulus induced their differentiation into three phenotypically, morphologically, and functionally distinct subsets, in the absence of cell division: P1 (PD-L1+CD80-), P2 (PD-L1+CD80+) and P3 (PD-L1-CD80+). Different stimuli induced variable proportions of the subsets, suggesting that steady state pDC are multipotent. P1-pDCs display a plasmacytoid morphology and strong specialization on IFN production, whereas P3-pDCs adopt a dendritic morphology and adaptive immune functions. P2-pDCs have an intermediate functional profile. We found that a P1-pDC phenotype is present in human autoimmune diseases associated to type I IFN production as lupus and psoriasis, supporting their pathophysiological relevance. We propose that peripheral innate activation represents a differentiation mechanism to generate subsets diversity and functional complementarity in human pDCs.

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Project description:Low capacity to produce reactive oxygen species (ROS) due to mutations in neutrophil cytosolic factor 1 (NCF1/p47phox) is strongly associated with lupus development both in humans and mouse models. Here, we aim to identify the major mechanisms of the Ncf1-disease association. We found that plasmacytoid dendritic cells (pDCs), the most potent producers of type I IFNs, exacerbate pristane-induced lupus in ROS-defective Ncf1-mutant and human NCF1-339 variant carrying mice. ROS deficiency in mouse models with Ncf1 mutation or human NCF1-339 variant leads to enhanced pDC generation via the TLR7/AKT/mTOR pathway and accumulation at sites of inflammation, resulting in an increased IFNα secretion. The produced IFNα further stimulates the JAK1/STAT1 pathway, which we found is hyperreactive in ROS-deficient pDCs. This, in turn, leads to increased type I IFN signature and enhanced proinflammatory responses. Our discoveries explain the causative effect of dysfunctional Ncf1 and pathogenicity of pDCs in lupus.

2023-03-12 | PXD035964 | Pride

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